ERCC1 ELISA Kit (DEIA-XYA612)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
cultured cells
Species Reactivity
Human, Mouse
Intended Use
The ERCC1 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor ERCC1 protein expression profile in cells. The kit can be used for measuring the relative amounts of ERCC1 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on ERCC1.
Contents of Kit
1. 96-Well Cell Culture Clear-Bottom Microplate: 1 plate
2. 10x TBS: 24 mL (10x), Clear
3. Quenching Buffer: 24 mL (1x), Clear
4. Blocking Buffer: 50 mL (1x), Clear
5. 10x Wash Buffer: 50 mL (10x), Clear
6. 100x Anti-ERCC1 Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
7. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
8. HRP-Conjugated Anti-Rabbit IgG Antibody: 6 mL (1x), Glass
9. HRP-Conjugated Anti-Mouse IgG Antibody: 6 mL (1x), Glass
10. Primary Antibody Diluent: 12 mL (1x), Clear
11. Ready-to-Use Substrate: 12 mL (1x), Brown
12. Stop Solution: 12 mL (1x), Clear
13. Crystal Violet Solution: 6 mL (1x), Glass
14. SDS Solution: 24 mL (1x), Clear
15. Adhesive Plate Seals: 4 seals
Storage
4°C/6 Months

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References


Tumor characteristics, expressions of ERCC1, Bax, p53, IGF1R, Bcl2, Bcl2/Bax and prognostic factors for overall survival in patients with lung carcinoid

JOURNAL OF BUON

Authors: Velinovic, Marta; Jankovic, Radmila; Jovanovic, Dragana; Trifunovic, Vesna Skodric; Gavrilovic, Dusica; Stojsic, Jelena; Cavic, Milena

Purpose: Neuroendocrine lung tumors (NET) include typical carcinoids (TC), atypical carcinoids (AC), large cell NE carcinoma (LCNEC) and small-cell carcinoma (SCLC), with different clinicopathological profiles and relative grades of malignancy. Although differences between carcinoids and high grade carcinomas are recognized, precise differences and behavior of TC and AC have not been clearly defined. The aim of this study was to better define the differences in the clinical behavior of TC and AC, and to establish new prognostic factors of overall survival (OS), by determining the levels of genetic expression of IGF1R, ERCC1, Bax, p53, Bcl2 and Bcl2/Bax ratio. Methods: The histopathological diagnosis of 52 surgically resected pulmonary carcinoid tumors was made according to the WHO classification. Gene expressions were evaluated by quantitative real-time PCR. Results: The confirmed prognostic factors for overall survival (OS) were pTNM T (p<0.01) pTNM N (p<0.05), clinical stage (p<0.05), type of surgery (p<0.01) and histopathological (HP) tumor type (p<0.05). Bcl2 mRNA level and Bcl2/Bax ratio were found to have a potential for discrimination of the HP type of tumor (AC vs TC, Receiver Operating Characteristics (ROC) cut-off values 0.1451 and 0.3015, respectively), but without statistically significant impact on OS. Conclusions: In patients with NETs, smaller primary tumor, absence of positive lymph nodes, and TC type of tumor predicted longer OS. Type of resection has influence on OS. Bcl2 expression and Bcl2/Bax ratio might be valuable as independent diagnostic parametars in lung carcinoids. Therapeutic approaches using attenuation of Bcl2 or upregulation of Bax might prove useful in lung NETs.

DNA repair efficiency associated with reprogrammed osteosarcoma cells

GENE REPORTS

Authors: Choong, Pei-Feng; Teh, Hui-Xin; Teoh, Hoon-Koon; Ong, Han-Kiat; Cheong, Soon-Keng; Kamarul, Tunku

Genomic instability and genetic heterogeneity are typical hallmarks of cancer, including osteosarcoma (OS), a type of bone tumor. Inactivation of DNA repair pathways may play an important role in the initiation and progression of OS pathogenesis by increasing the mutation rate and genomic instability. However, there is still a lack of information on gene alterations and mutations that may increase the risk of osteosarcoma formation. Reprogramming OS cells to a primitive stage namely induced pluripotent stem cell (iPSC) state could be a useful disease model to understand the pathogenesis of OS and to bridge the current gap of knowledge on DNA repair mechanisms in reprogrammed OS cells. By using Yamanaka factors, OS cell lines, G-292 and Saos-2, were reprogrammed to iPSC lines, respectively iG-292 and iSaos-2, both of which demonstrated pluripotency similar to embryonic stem cells. However, only iG-292 was able to form teratoma. Subsequent microarray data showed significant down-regulation of DNA Damage Response (DDR) genes expression for both iG-292 and iSaos-2. A functional assay using UV-induced DNA damage approach demonstrated efficient DNA repair mechanism in iG-292. Further analysis of nucleotide excision repair (NER) genes demonstrated up-regulation of GADD45G, XPA, RPA, MNAT1, ERCC1, PCNA, and POLL, in iG-292. Up-regulation of GADD45G together with up-regulation of other NER genes synergistically repair UV damage by rapid removal of cyclobutane pyrimidine dimers. In conclusion, down-regulation of DDR genes in reprogrammed OS may render an enhanced state of genomic integrity in reprogrammed OS as compared to the parental cells. Thus, this study demonstrated for the first time DDR profile of reprogrammed OS cells and the probable involvement of GADD45G in the DNA repair mechanism of reprogrammed OS cells.

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